Brain-Heart Afferent-Efferent Traffic

Dusi, Veronica; Jeffrey, L. Ardell.

doi:10.1007/978-3-030-28008-6_2

Cited by 10 publications

(8 citation statements)

References 210 publications

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“…Although most patients will not have a cardiac cause, all patients should be evaluated to ensure the early identification or exclusion of life-threatening causes [ 14 ]. The exact mechanism by which myocardial ischemia causes chest pain remains obscure but chemical and mechanical stimulation of sensory afferent nerve endings in the coronary arteries and myocardium is now recognized as a major factor in the progression of cardiac angina [ 15 ]. The nociceptive C-fibers of the spinal cardiac afferent fibers arising from dorsal root ganglions are dispersed throughout the ventricle, expressing a variety of ion channels or receptors and contributing to the processing of general cardiac nociception [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

Cervical Radiculopathy as a Hidden Cause of Angina: Cervicogenic Angina

Chu

2022

J Med Cases

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Patients presenting with chest pain to the emergency department constitute a diagnostic challenge as 77% of the patients' symptoms are not cardiac. Diagnostic uncertainty is a pervasive issue in primary care. A 56-year-old man presented with non-traumatic chest pain and chronic neck pain for 2 years, as well as numbness in his right third and fourth fingers for 6 months. It was not associated with palpitation, orthopnea or pedal edema. Except for hyperglycemia, no abnormal findings were found in diagnostic tests. At that time, he was being treated for type 2 diabetes using glucose-lowering drugs in order to lower his blood glucose and lessen his risk of heart disease. The cause of his chest pain remained unknown. Following a second opinion from an orthopedist, the patient was diagnosed with cervical radiculopathy and was treated with analgesics and physical therapy. Because the treatments had only provided temporary pain relief for the previous 6 months, he sought chiropractic care for pain relief. The patient's vital signs were stable and within normal limits during the assessment. A restricted neck movement, a positive Spurling test, and hypoesthesia in the right C7 dermatome were seen. Cervical radiographs revealed degenerative spondylosis with right C5/C6 neuroforaminal stenoses and bilateral C6/C7 neuroforaminal stenoses. A provisional diagnosis of cervical spondylotic radiculopathy associated with cervicogenic angina (CA) was made. Chiropractic procedures, including cervical manipulation, instrumented soft tissue mobilization, and motorized intermittent neck traction, were performed two to three times per week. After 3 months, the patient reported that the chest pain, neck pain, and radicular symptoms had completely resolved. Repeated radiographs taken during the 11th month followup revealed a comparable improvement in the increased spacing of the restricted neuroforamina, which could signify a beneficial alteration related to cervical function retrieval. CA is an angina-like chest pain caused by cervical spine disorders. This study adds to our understanding of the biomechanical impact of cervical radiculopathy on chest pain, which has largely been overlooked during diagnostic workups. Once cervical radiculopathy has been identified, CA symptoms can be eased by alleviating the noxious input stemming from the pinched nerve roots.

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Section: Discussionmentioning

confidence: 99%

Cervical Radiculopathy as a Hidden Cause of Angina: Cervicogenic Angina

Chu

2022

J Med Cases

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“…Among other neurotransmitters, the parasympathetic postganglionic terminal also releases NO, whose presynaptic action facilitates the release of ACh and inhibits that of NE, while at the postsynaptic level, it negatively modulates HCN channels [92], and VIP, which, opposite to ACh, increases cAMP concentration via VPAC1 and VPAC2, as an autoregulatory mechanism of signaling [93]. Beyond the well-characterized negative impact on chronotropism, vagal activation typically decreases several other cardiac indices including atrial contractility, atrial effective refractory period (AERP) duration (in an inhomogeneous way, therefore significantly increasing atrial refractoriness dispersion), AV conduction and ventricular contractile force [94]. While the negative chronotropic effect largely relies on a different intracellular pathway (IKACh current activation), which is the main responsibility for the different kinetics of sympathetic and parasympathetic chronotropic control, all the other effects mostly reflect cAMP inhibition, and therefore have an opposite intracellular effect compared to catecholamines, with an expected similar time onset of the effect.…”

Section: The Parasympathetic-neurocardiac Junctionmentioning

confidence: 99%

The Intrinsic Cardiac Nervous System: From Pathophysiology to Therapeutic Implications

Giannino,

Braia,

Griffith Brookles

et al. 2024

Biology

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The cardiac autonomic nervous system (CANS) plays a pivotal role in cardiac homeostasis as well as in cardiac pathology. The first level of cardiac autonomic control, the intrinsic cardiac nervous system (ICNS), is located within the epicardial fat pads and is physically organized in ganglionated plexi (GPs). The ICNS system does not only contain parasympathetic cardiac efferent neurons, as long believed, but also afferent neurons and local circuit neurons. Thanks to its high degree of connectivity, combined with neuronal plasticity and memory capacity, the ICNS allows for a beat-to-beat control of all cardiac functions and responses as well as integration with extracardiac and higher centers for longer-term cardiovascular reflexes. The present review provides a detailed overview of the current knowledge of the bidirectional connection between the ICNS and the most studied cardiac pathologies/conditions (myocardial infarction, heart failure, arrhythmias and heart transplant) and the potential therapeutic implications. Indeed, GP modulation with efferent activity inhibition, differently achieved, has been studied for atrial fibrillation and functional bradyarrhythmias, while GP modulation with efferent activity stimulation has been evaluated for myocardial infarction, heart failure and ventricular arrhythmias. Electrical therapy has the unique potential to allow for both kinds of ICNS modulation while preserving the anatomical integrity of the system.

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“…In the last 50 years, our understanding of the anatomical and functional organization of cardiac neuraxis has dramatically improved. 11 Cardiac neuronal control is realized through a series of reflex control networks involving somata in the (i) intrinsic cardiac ganglia (heart), (ii) intrathoracic extracardiac ganglia (stellate, middle cervical), (iii) superior cervical ganglia, (iv) spinal cord, (v) brainstem, and (vi) higher centres. Each one of these processing centres harbours afferent, efferent, and local circuit neurons, which interact both locally and in an interdependent fashion with the other levels to orchestrate electrical and mechanical local cardiac indices on a beat-to-beat basis.…”

Section: The Premisesmentioning

confidence: 99%

Sympathetic activation in heart failure

Gronda

Dusi

D’Elia

et al. 2022

European Heart Journal Supplements

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Sympathetic activation has been long appreciated exclusively as a fundamental compensatory mechanism of the failing heart and, thus, welcome and to be supported. In the initial clinical phases of heart failure (HF), the sympathetic nervous system overdrive plays a compensatory function aimed at maintaining an adequate cardiac output despite the inotropic dysfunction affecting the myocardium. However, when the sympathetic reflex response is exaggerated it triggers a sequence of unfavourable remodelling processes causing a further contractile deterioration that unleashes major adverse cardiovascular consequences, favouring the HF progression and the occurrence of fatal events. Eventually, the sympathetic nervous system in HF was demonstrated to be a ‘lethality factor’ and thus became a prominent therapeutic target. The existence of an effective highly specialized intracardiac neuronal network immediately rules out the old concept that sympathetic activation in HF is merely the consequence of a drop in cardiac output. When a cardiac damage occurs, such as myocardial ischaemia or a primary myocardial disorder, the adaptive capability of the system may be overcame, leading to excessive sympatho-excitation coupled with attenuation till to abolishment of central parasympathetic drive. Myocardial infarction causes, within a very short time, both a functional and anatomical remodelling with a diffuse up-regulation of nerve growth factor (NGF). The subsequent nerve sprouting signal, facilitated by a rise in the levels of NGF in the left stellate ganglion and in the serum, triggers an increase in cardiac nerve density in both peri-infarct and non-infarcted areas. Finally, NFG production decreases over time, supposedly as an adaptative response to the prolonged exposure to sympathetic overactivity, leading in the end to a reduction in sympathetic nerve density. Accordingly, NGF levels were markedly reduced in patients with severe congestive heart failure. The kidney is the other key player of the sympathetic response to HF as it indeed reacts to under-perfusion and to loop diuretics to preserve filtration at the cost of many pathological consequences on its physiology. This vicious loop ultimately participates to the chronic and disruptive sympathetic overdrive. In conclusion, sympathetic activation is the natural physiological consequence to life stressors but also to any condition that may harm our body. It is the first system of reaction to any potential life-threatening event. However, in any aspect of life over reaction is never effective but, in many instances, is, actually, life threatening. One for all is the case of ischaemia-related ventricular fibrillation which is, strongly facilitated by sympathetic hyperactivity. The take home message? When, in a condition of harm, everybody is yelling failure is just around the corner.

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Brain-Heart Afferent-Efferent Traffic

Cited by 10 publications

References 210 publications

Cervical Radiculopathy as a Hidden Cause of Angina: Cervicogenic Angina

Cervical Radiculopathy as a Hidden Cause of Angina: Cervicogenic Angina

The Intrinsic Cardiac Nervous System: From Pathophysiology to Therapeutic Implications

Sympathetic activation in heart failure

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